Our findings were mostly consistent with those hypothesized and the null hypotheses were largely rejected.
It was therefore hypothesized that RIIB null (RIIβ−/−) mice would express anti-aging phenotypes.
Rb-heterozygous mice were also predisposed to tumor development, although they did not have retinoblastoma as initially hypothesized, and Rb-null animals died at early embryonic stages.
Considering the nature of the movement abnormality we hypothesized that GALT-null flies might have an anatomical defect visible in brain or muscle, and so performed the following histological studies.
For example, it can be hypothesized that, in VDR null mice, satellite cells may be anomalously activated, proliferate, and differentiate to form new myonuclei that fuse with existing fibers to restore normal fiber size.
Because misclassification of an outcome or exposure usually (although not invariably) biases measures of association towards the null, we hypothesized that the magnitude of risk (measured as adjusted odds ratios [aOR] with 95percentt confidence intervals [CI]) for known risk factors would move further from unity with less misclassification.
In view of this result, we hypothesize that a null allele of Ncras FlbE would also display a wild type phenotype in terms of conidiation.
Within this area of near-universal ITN coverage, we hypothesize that our null results are explained in part by the community effect of ITNs, where children unprotected by ITNs benefited from an overall suppression of transmission.
*Positive or partially positive finding coded as "1", Null or against hypothesized finding coded as "0" (referent category).
Given the essential role of PPARγ in adipocyte differentiation [12], [13], and the abnormalities observed in specific layers of PPARγ-null placentas, we hypothesized that PPARγ also regulates critical aspects of normal trophoblast differentiation.
